Prostate cancer is one of the most common cancers in men. Unfortunately, it is also the second leading cause of death from cancer in men in the United States. The treatment or therapy for prostate cancer usually involves surgery, chemotherapy, and radiation. Due to these treatments, there are noticeable adverse effects on the patients during and after the treatment. However, bioactive ingredients extracted from food resources can provide parallel as well as additional approaches to treat prostate cancer.  

Fucoidan is a sulfated polysaccharide obtained mainly in various species of brown algae and brown seaweed. It is reported that Fucoidan has antitumor activity on different cancer cells. Compared to medication, Fucoidan is a food-grade ingredient that can provide complementally and alternative strategies without intolerable side effects. In a previous study, ‘Fucoidan induced apoptosis of PC-3 human prostate cancer cells in Vitro, the possible role in vivo was still unknown. Hence, I want to share the following study that investigated the antitumor and anti-angiogenesis effects of Fucoidan.

According to “Antitumor and anti-angiogenetic effects of Fucoidan on prostate cancer: possible JAK-STAT3 pathway” by Xin Rui et al., they treated DU-145 cells (Human prostate cancer cells) with different Fucoidan concentrations (100~100 μg/mL) to assess additive-free culture DU-145 for its possible cell proliferation effect and cell survival rate. As for the result, Fucoidan inhibited the viability of DU-145 cells in a dose-independent manner significantly (Fig1).

Researchers examined using each respective culture kit to assess the invasive ability and angiogenetic potential of DU-145. And we found that treatment of Fucoidan inhibits DU-145 invasion and angiogenesis (Fig. 2).

Subsequently, for clarifying the antitumor effect of Fucoidan on prostate cancer cells in vivo, DU-145 cells were injected subcutaneously into athymic nude mice and treated with saline or fucoidan (20mg/mL) by oral administration for 28 days. Following that, tumor weight was measured every four days. As a result, Fucoidan inhibited tumor growth of prostate cancer xenograft (Fig. 3).

Researchers have not indicated data in this paper. Yet, they analyzed xenograft tumors by hemoglobin assay and found that Fucoidan significantly decreased hemoglobin content compared with control. We found that mRNA expression levels of CD3 and CD105 in tumor tissue were also declined after fucoidan treatment. From these data, it suggested a possibility that Fucoidan hindered tumor growth by inhibiting angiogenesis.  

As they know JAK-STAT3 pathway is involved in angiogenesis or tumor invasion and metastasis. Researchers examined the protein expression in Western bolt’s tumor tissue and found that phosphorylated JAK and STAT3 were reduced after treatment. Next, they performed ChIP to investigate the change of STAT3-regulated gene promoters in the xenograft. The activation of VEGF, Cyclin D1, Bcl-xL promoters was also significantly reduced after treatment (omit data).

Taken together, they first disclosed the antitumor and anti-angiogenetic effect of Fucoidan on prostate cancer in both cell-based assay and mouse xenograft model. Researchers clarified the role of the JAK-STAT3 pathway in the protection. All these findings provided innovative complementary and alternative strategies to treat prostate cancer. 

Reference: The JAK-STAT signaling pathway is a chain of interactions between intracellular proteins and is involved in processes such as immunity, cell division, cell death, and tumorigenesis.